Diarrhea, “Answers” from EM Lyceum


Acute gastrointestinal disorders are some of the most frequent problems evaluated by ED physicians.  Complaints of diarrhea account for almost 5% of visits to the emergency departments (Bitterman, 1988).  Although the disease entity is extremely prevalent and current evidence on the subject is nothing short of “voluminous,” practice differences among ED physicians in its evaluation and management are as varied and inconsistent as the stools themselves.
1. When do you send stool cultures, stool ovum and parasites, and/or fecal WBC? How do you use the results in diagnosis and management?
EML Diarrhea Answers
Stool evaluation of fecal leukocytes (WBC) and occult blood is sent in many ED’s as a positive result has traditionally been thought to be predictive of either an inflammatory or infectious etiology of the diarrhea. Fecal WBC’s and RBC’s are generally found in stool infected with invasive bacterial pathogens such as Salmonella, Shigella, Campylobacter, Enteroinvasive E-coli, Enterohemorrhagic E-col( E-coli 0157-H7), but also in stools of patients with inflammatory disorders such as Crohn’s disease, Ulcerative Colitis, and pseudomembranous colitis. Studies show a sensitivity for predicting bacterial infection for fecal WBC ranging from 40% (Chitkara, 1996) to 73% (Thielman, 2004). Fecal WBC testing also appears to have a specificity of approximately 85% (Thielman, 2004) for bacterial pathogens.
Many studies have demonstrated that fecal occult blood testing (FOBT) is nearly equivalent in sensitivity to fecal WBC in predicting the presence of an invasive bacterial pathogen. One large, well-designed study of 1040 patients with acute diarrhea found that a negative FOBT had a negative predictive value of 87% for invasive bacterial pathogens (McNeely, 1996). Another large study of 446 children demonstrated an 88% sensitivity for the combination of bloody diarrhea by history, positive fecal WBC and positive FOBT for predicting a bacterial pathogen  (Huicho, 1993).
Underpinning the problems inherent in many of these studies is that the gold standard for determining sensitivities, specificities and predictive values was often stool cultures, which themselves have not been shown to be the greatest of tests (as we will discuss). What do we do with these results then, you ask? Well, there is no consensus on when to order fecal WBC or occult RBC’s, however, guidelines by the Infectious Disease Society of America (IDSA) and the American Association of Gastroenterology (AAG) recommend a selective approach since most run-of-the-mill cases of infectious diarrhea are viral in etiology, self-limiting and do not require any testing. They recommend testing patients at high risk for invasive bacterial pathogens (fever > 101.3, severe, or persistent diarrhea (> 7 days), severe abdominal pain, bloody diarrhea, the immunocompromised, elderly or systemically ill patients) (Guerrant, 2001).
Stool cultures, though frequently ordered in the ED, are notoriously poor at identifying bacterial pathogens as a result of their relatively low yield. In six studies conducted between 1980 and 1997 only 1.5%-5.6% of cases grew positive stool cultures. This results in a cost of about $1000 for each positive culture (Guerrant, 2001). Similar low yields have been duplicated by other studies as well. Most people are also unaware that routine stool cultures in most laboratories don’t test for ALL possible pathogens, but primarily identify Shigella, Campylobacter, and Salmonella only.  All other bacteria, including E-coli O157-H7 usually require special requests. As a result, most guidelines also recommend only sending stool cultures in high-risk patients (as denoted above), plus those with positive fecal WBC/occult blood, or those patients being admitted for their diarrhea. The vast majority of patients will not require stool cultures (Dupont, 2014).
Lastly, in developed countries, routine use of stool ova and parasite testing is rarely indicated (Siegel, 1990). Primarily it is used to help identify diarrhea caused by parasites including Giardia, EntamoebaCyclospora and Cryptosporidium. As these pathogens are relatively rare in the US, only consider sending these tests in travelers recently returning from Russia (Giardia and Cryptosporidium) or the mountainous regions of North America (Giardia), in AIDS-associated diarrhea (Cryptosporidium), those exposed to infants at a daycare center (Giardia and Cryptosporidium), or longstanding diarrhea not responsive to antibiotic therapy. If you clinically suspect any of these pathogens be sure to send multiple samples for stool ova and parasites to improve the yield, as parasite excretion may be intermittent.
Bottom line: It is prudent to order fecal WBCs as a screening test in high risk patients (denoted above), as it may help you determine the presence of an invasive bacterial pathogen, but in these patients an FOBT may be easier, cheaper, and just as good.  Stool cultures should be sent if fecal WBC/RBC testing is positive, or if patients are being admitted for their diarrhea. Stool O&P is rarely indicated or cost-effective in the US except for very few special circumstances (denoted above).  
2. When do you get bloodwork? When do you pursue imaging?
Most patients who present to the ED with acute diarrhea will have a self-limited disease course. However, many physicians often reflexively order a set of basic labs in these patients to check for any “electrolyte disturbances” from the presumed water loss. Many studies have shown that routine blood work in these patients is unnecessary. In a study by Olshaker, et al., 281 adult patients with acute gastroenteritis were retrospectively reviewed and only 1% of patients were found to have a clinically significant electrolyte abnormality that required treatment or affected disposition. None of the patients with acute gastroenteritis alone had electrolyte abnormalities. They also found that the time spent in the ED was 3-4 times longer for those patients who had electrolytes ordered (Olshaker, 1989).
Routine CBC is also unnecessary in most patients with acute diarrhea as an elevated WBC is non-specific. A hemoglobin level may be appropriate in cases of large amounts of bloody diarrhea. A platelet count may be helpful in children with bloody diarrhea in which you are concerned about Hemolytic Uremic Syndrome (HUS) as a further complication, but otherwise these tests are largely unhelpful.
So does this mean we should never order routine lab work on anyone with acute diarrhea? Not necessarily. The above description and evidence is primarily true for cases with a self-limited diarrhea that is likely due to a viral or non-invasive bacterial pathogen (the majority of patients seen in the ED). In the smaller subgroup of patients with risk-factors for invasive bacteria (i.e., high fever, severe or persistent diarrhea (> 7 days), severe abdominal pain, bloody diarrhea, positive fecal WBC or fecal occult blood, the immunocompromised, elderly, or systemically ill/toxic appearing patients), obtain at least a CBC and BMP to assist with your evaluation and treat any electrolyte abnormalities that may be present (Dupont, 2014).
Similarly, most patients seen in the ED with acute diarrhea do not need any imaging to be performed.  It is important, however, to expand your differential diagnosis outside of infectious etiologies of diarrhea to identify the subset of patients at risk for other pathologies for whom further imaging may be warranted.
For example, patients with appendicitis may also present with diarrhea.  Usually vomiting and diarrhea precede abdominal pain in infectious diarrhea, whereas vomiting often follows abdominal pain in patients with appendicitis.  In a study of 181 children < 13yrs old who were eventually discovered to have appendicitis, 27% were initially misdiagnosed, and many of those children presented with diarrhea as an initial symptom (Rothrock, 1991).  Ischemic bowel disease should also be on the differential diagnosis in elderly patients with severe abdominal pain and a history of vascular disease as these patients may also present with occasional diarrhea and bloating (Tabrez, 2001).  If ischemic bowel disease is being considered, a contrasted CT of the abdomen and pelvis should be ordered.  Furthermore, small bowel obstruction and diverticulitis can often present with diarrhea, but may not be diagnosed unless formal imaging is obtained.
Be extra cautious in evaluating elderly patients with diarrhea and abdominal pain as these patients tend to have more serious, often surgical, illnesses that present atypically or go unrecognized longer (Hendrickson, 2003).
Bottom line: most patients seen in the ED with acute diarrhea require no routine blood work unless the patient has high-risk features. Imaging is also usually not necessary unless you are considering other diagnoses including appendicitis, mesenteric ischemia, small bowel obstruction, and diverticulitis.  
3. Which patients do you treat with antibiotics?
Whether or not to prescribe antibiotics and to which patients is one of the most controversial and most discussed aspects of the management of diarrhea. Analyzing all the evidence currently available is enough to cause one to have diarrhea in and of itself, but fear not. Let’s break it down in pieces . . .
Why give antibiotics in the first place, you ask, if many of these disease processes are self-limited?  In various studies, antibiotics appear to decrease the length of the diarrhea symptoms by about 24-48 hrs regardless of whether the diarrhea was guiac positive, fecal WBC positive, or had positive stool cultures  (Guerrant, 2001Dryden, 1996Wistrom 1992).  The moderately to severely ill seem to benefit more from antibiotics.  Why would antibiotics decrease symptoms in culture negative stools? Some believe the antibiotics are eradicating bacterial pathogens that stool cultures were unable to detect. Traditionally it was thought that antibiotics may not be beneficial in mild-moderate diarrhea, due to their tendency to prolong the carrier state, especially amongst those infected with Salmonella.  However, newer studies show and that carrier rates are approximately equivalent in those treated with or without antibiotics (Dryden, 1996).
So now that we understand why we may give antibiotics, the question becomes who we should give them to? Many experts argue that most patients, regardless of symptoms and lab test results, don’t need antibiotics since most acute diarrheal illnesses are self-limited.  Additionally, further prescription of antibiotics will lead to increased drug resistance and side-effects. Other guidelines, including those from the IDSA and AAG, provide a more conservative approach. They state patients should receive antibiotics if they are presenting with symptoms of traveler’s diarrhea, as immediate treatment can reduce symptom duration by 2-3 days (Guerrant, 2001).  They further recommend antibiotic therapy in those patients with high fever (>101.3), history suspicious of a moderate-severe bacterial infection, guiac positive stools or positive fecal WBC (Guerrant, 2001).  Some criticize the IDSA guidelines for relying too heavily on stool testing to decide whether or not to give antibiotics.
Just as important as knowing which patient to give antibiotics to is knowing which patients to be cautious about giving antibiotics. In general, antibiotics are not advised for the treatment of diarrhea in most pediatric patients.  The cornerstone of treatment in pediatric patients is fluid replacement. Inadequate fluid replacement leads to the 9% of hospitalizations in children < 5 yrs of age caused by diarrhea (Cicirello, 1994).  Caution is also advised in prescribing antibiotics in patients with grossly bloody diarrhea.  This is because one of the common causes of grossly bloody diarrhea is Enterohemorrhagic E-coli (AKA E-coli 0157-H7).  Various studies (including one published in the New England Journal of Medicine in 2000) demonstrated higher risk of HUS in pediatric patients with EHEC who were treated with antibiotics (Wong, 2000).  There is also concern that elderly patients with EHEC may develop TTP if treated with antibiotics.
If you decide to give antibiotics to a patient with an acute diarrheal illness, which antibiotics should you give? Most studies and current guidelines recommend ciprofloxacin to help eradicate acute bacterial pathogens. Two basic regimens exist, either a one-time dose of ciprofloxacin 1gm or a regimen of ciprofloxacin 500mg twice/day x 3 days.  Some regimens use macrolides, as fluoroquinolones will not be effective in cases of Campylobacter (Dupont, 2014).
Bottom line: In most cases of watery diarrhea, no antibiotics are needed as the disease is usually self-limiting. When there is concern for invasive disease (positive fecal WBCs or RBCs, or young, adult, healthy patients with grossly bloody stools), it may be reasonable to prescribe ciprofloxacin 500mg BID x 3 days to help reduce symptoms by 24-48 hours (although many sources argue that this is unnecessary)Also, be cautious in giving antibiotics to pediatric and elderly patients with grossly bloody diarrhea as HUS and TTP are concerns.       
4. What other medications do you use? Loperamide, Lomotil, Pepto? What about probiotics?
Loperamide (Imodium) is a peripheral opioid receptor agonist that acts on the mu-opioid receptors in the myenteric plexus of the large intestine without affecting the mu-receptors in the CNS. It works by slowing gastrointestinal motility, thereby allowing more time for fluid and electrolytes to be absorbed from the fecal material. Loperamide is generally considered to be safe in most acute infectious diarrhea in patients who are afebrile and have non-bloody diarrhea and those individuals with chronic diarrhea from inflammatory bowel disease (Gore, 2003).
In those with more severe illnesses (immunocompromised, bloody diarrhea, fever > 101.3), some experts believe the use of Loperamide will allow the invasive bacteria to remain in the gut for a longer period of time and potentially worsen the acute diarrheal illness. However, there is evidence that supports the use of Loperamide in sicker patients in combination with antibiotics. In two studies, one in Thailand on patients with dysentery and another amongst US soldiers with traveler’s diarrhea, the use of Loperamide effectively reduced the number of loose bowel movements compared to placebo when given in adjunct with ciprofloxacin (Petrucelli, 1992Murphy 1993).
Loperamide may increase the risk of HUS in pediatric patients (Guerrant, 2001Cimolai, 1990) and many guidelines advise against the use of anti-motility agents in pediatric patients.
Lomotil (diphenoxylate/atropine) is a combined opiate-agonist (diphenoxylate) and anticholinergic (atropine) agent that is also available as an adjunct for symptomatic treatment of diarrhea. The diphenoxylate component acts on the mu-receptors of the gut wall in a similar fashion to Loperamide, however, its mu effects are not restricted to the periphery and may cross into the CNS. As a result, atropine is combined in the medication to discourage overdose. From the drug description alone, it can be seen that this medication may be more dangerous and habit-forming than Loperamide in treating the acute symptoms of diarrhea. Diphenoxylate has not been studied in any randomized clinical trials and is not recommended by many experts for symptomatic treatment of acute diarrhea.
Bismuth subsalicylate, sold most commonly under the brand name Pepto-Bismol functions as an anti-secretory, anti motility agent with some weak but present bactericidal properties. As it is a salicylate, its toxicologic considerations, especially in pediatric patients, require extreme caution and likely avoidance in small children out of concern for at home dosing misadventures. Very little rigorous study of Pepto exists, with some volunteer reports of its use in traveler’s diarrhea in military personnel decreasing symptoms subjectively (Putnam, 2006). One double-blinded randomized study of Bangladeshi children aged 4-36 months found a modest improvement in acute diarrheal illness (Chowdhury, 2001). AN open label study in volunteers found loperamide to be faster and more effective than Pepto in adults (Dupont, 1990). Pepto, though, may be particularly useful in cases of norovirus, a common cause of acute diarrhea (Pitz, 2015). If toxicity is avoided in dosing, there is little downside in including this in a patient’s antidiarrheal armamentarium.
Probiotics are live organisms found in a variety of foodstuffs that have been used to help colonize the intestine with “good bacteria” to prevent or treat both infectious and antibiotic associated diarrhea. Lactobacillus is one of the most widely available and studied of these probiotics. In the Cochrane Review of over 23 studies involving over 1900 adults and children, probiotics were found to reduce the overall risk of having diarrhea at 3 days by approximately 35% and reduced the duration of the diarrhea by approximately 30 hours (Allen, 2004). Multiple other studies show similar results while also demonstrating a good safety profile.
In regards to the use of probiotics in the prevention of antibiotic-associated diarrhea, the largest meta-analyses was conducted in 2012 (62 studies, 11,000 patients). A majority of the included studies used Lactobacillus as the probiotic and found a 42% lower risk of developing antibiotic associated diarrhea than control groups (RR 0.58, 95% CI 0.5-0.68) with a number needed to treat (NNT) of 13 to prevent one case of antibiotic associated diarrhea (Hempel, 2012).
Bottom line: Loperamide (Imodium) may be useful and safe in most cases of acute diarrhea, however, some caution should be advised in the severely ill and in and those with bloody diarrhea unless an antibiotic is concurrently prescribed. Loperamide should be avoided in pediatric patients. Lomotil is not recommended for symptomatic relief. Probiotics (specifically Lactobacillusare showing promising evidence for their use in the prevention and treatment of both infectious and antibiotic associated diarrhea.    
Author: Bhandari  Editors: Swaminathan, Bryant
Check out EM Lyceum page for more such reviews. 

Originally posted by EM Lyceum on 2/11/2015. Re-Posted with Permission. 

Transient Global Amnesia

Recently, I was taking care of an elderly female who presented to the ED with isolated amnesia. I thought of some rare stroke syndrome until she was seen by a Neurology attending who called it "Transient Global Amnesia". I was not even aware of this diagnostic entity. 

What is Transient Global Amnesia (TGA)?
Transient global amnesia (TGA) is syndrome characterised by the acute onset of anterograde or retrograde amnesia that can last up to 24 hours in the absence
 of other neurologic deficits. TGA exhibits isolated loss of new memory formation limited to facts and events and patients retain motor tasks and coordination. The classic TGA patient asks the same questions repeatedly in the absence of other signs or symptoms. However, symptoms resolve gradually and spontaneously within 24 hours without the need for medical intervention. The definitive diagnosis of TGA cannot be made until symptoms have resolved. 




How does TGA present?
The classic TGA patient asks the same questions repeatedly in the absence of other signs or symptoms. They exhibit anterograde memory loss. For instance, a patient might repeatedly ask "Have we met before" despite several introductions. Other common concurrent symptoms seen with TGA are headache, nausea, and vomiting. 

What are they key points to cover while examining a suspected TGA?
Do a full neurological exam (Cranial Nerves, Sensory-Motor, Cerebellum, Reflexes). Memory function forms a crucial part of the examination as patients with TGA experience explicit memory loss i.e only the loss of memory pertaining to new facts and events (mainly stored by the hippocampus). By contrast, implicit memories (stored in the cerebellum and the basal ganglia) should not be compromised. For example, a TGA patient retains the ability to operate a car or the ability to open a door with a key. Patients also retain all other cognitive functions. 


1. Test immediate versus delayed recall. Immediate recall remains intact in TGA patients, while delayed recall (after 5 minutes) is impaired.
2. Assess attention span. Executive function abilities such as “serial 7s” or spelling the word “world” backwards remains intact during TGA.
3. Test procedural memory. TGA patients retain task memory (eg, making a paper airplane).
4. MMSE


What is the diagnostic criterion for TGA?
  1. Witnessed at onset and during attack
  2. Must have anterograde amnesia

  3. No focal neurological symptoms or signs during or after

  4. No epileptic features
  5. No clouding of consciousness, no loss of personal identity, and no cognitive impairment other than amnesia

  6. No head injury in the past 72 hours

  7. No seizures in the last 2 years, and not on medication for epilepsy
  8. Must resolve in 24 hours

Differentials for TGA
  • Seizure/transient epileptic amnesia 
(lasts < 1 hour)
  • Stroke (rarely presents as isolated amnesia) 

  • Atypical migraine 

  • Head injury/occult trauma/concussion syndrome 
(Manage as Head Injury)
  • Medication and recreational drug side effect 

  • Herpetic encephalitis 
(fails to resolve in <24hrs)
  • Early neurosyphilis 

  • HIV dementia 

  • Alcohol psychosis 
  • Alcohol blackout 



TGA cannot be definitely diagnosed unless and until all symptoms have resolved in under 24 hours. 

What are the risk factors for TGA?

  • Past history of TGA
  • Advanced Age
  • Migraneous Headaches

Diagnostic Tests
The yield of extensive diagnostic testing in search of occult etiologies is low if history is not concerning and examination is normal. However, certain high-risk patients require extensive workup. Imaging is warranted only if examination is concerning  and when the duration of symptoms approaching 24 hours without resolution of symptoms. MRI is preferred over CT whenever possible to rule out an unusual neurological syndromes. If there is any suspicion of an acute ischemic stroke, immediate computed tomography (CT) should be obtained. EEG can be done to rule in seizures.
Any patient with suspects TGA that does not resolve in 24 hours requires a broader investigation (MRI/CT, LP, EEG), admission, and neurologic consultation.

Who needs a extensive work up?
  • Absence of witness at onset
  • Patients aged < 50 years warrant special consideration, as TGA is rare in young individuals
  • High risk - Immunocompromised, Age<50, drugs/alcohol use, Abnormal Vital Signs

Treatment
  • Administer Thiamine if there is h/o chronic alcoholism
  • Hold medications that may explain amnestic symptoms (BZDs)
  • Admit in ED Observation unit or as an in-patient for 1-2 days and watch until resolution of symptoms
  • Mainstay of Rx is serial neuro examinations until the patient returns to baseline
  • Neurology Consultation 
Most TGA syndromes resolve in < 10 hours. Patients should be observed until symptoms clear. Patients with presumed TGA do not have decisional capacity and therefore must not be permitted to be discharged against medical advice while symptoms are present.



Take Home:

  • TGA is characterised by the acute onset of amnesia that can last up to 24 hours in the absence
 of other neurologic deficits. Symptoms resolve gradually and spontaneously within 24 hours without the need for medical intervention. 
  • The definitive diagnosis of TGA cannot be made until symptoms have resolved. 
  • For a classic case, do minimum tests but pay special attention  to high-risk individuals as well as any patient with abnormal vital signs or unusual symptoms.

References:

  1. Faust JS, Nemes A. Transient Global Amnesia: Emergency Department Evaluation And Management. Emergency medicine practice. 2016 Aug;18(6):1.
  2. Hodges JR, Warlow CP. Syndromes of transient amnesia: towards a classi cation. A study of 153 cases. J Neurol Neu- rosurg Psychiatry. 1990;53(10):834-843.
  3. Hodges JR, Ward CD. Observations during transient global amnesia. A behavioural and neuropsychological study of ve cases. Brain. 1989;112 (Pt 3):595-620.
  4. Brown J. ED evaluation of transient global amnesia. Ann Emerg Med. 1997;30(4):522-526. 
  5. Quinette P, Guillery-Girard B, Dayan J, et al. What does transient global amnesia really mean? Review of the litera- ture and thorough study of 142 cases. Brain. 2006;129(Pt 7):1640-1658.
  6. The transient global amnesia syndrome. JAMA. 1966;198(7):778-779. 


Posted by:


              
     Lakshay Chanana
     
     Speciality Doctor
     Northwick Park Hospital
     Department of Emergency Medicine
     England

     @EMDidactic

Atrial Fibrillation – ED Management

Pathophysiology
AF is a supraventricular tachycardia that arises from disorganized atrial depolarisation. Electrical remodelling results in multiple reentry circuits or rapidly ring atrial foci and shortening of atrial refractoriness and action potential contributing to the maintenance of AF. Patients with a fast ventricular rate need rate-control medications that slow down the conduction through AV node. 





EKG Findings in AF
  • Presence of low-amplitude brillatory waves on ECG without de ned P-waves
  • Irregularly irregular ventricular rhythm
  • Fibrillatory waves typically have a rate of > 300 beats per minute
  • Ventricular rate is typically between 100 and 160 beats per minute





Why should we treat AF with rapid ventricular rate in a stable/asymptomatic patient?
A persistently elevated ventricular rate during AF (usually > 120 beats/min) for prolonged time periods may result in mitral regurgitation, eventually leading to a dilated ventricular cardiomyopathy (tachycardia-induced cardiomyopathy).



Causes of AF
  • HTN
  • Thyrotoxicosis
  • Acute alcohol intoxication
  • ASD
  • IHD
  • Pericarditis
  • Myocardial Contusion
  • Valvular Heart Disease
  • Pulmonary Embolism
  • Pneumonia
  • Sepsis
  • Digoxin Toxicity
  • Obesity
  • Hypothermia
  • Pre-excitation Syndromes (WPW)


ED Management
The goals of AF management revolve around achieving hemodynamic stability, symptomatic treatment for fast ventricular rate, and the prevention of thromboembolic complications. This post is limited to attaining symptomatic treatment and hemodynamic stability. Use of clinical decision rules regarding the need for oral anticoagulation is not addressed here. 


Who needs immediate Electrical Cardioversion?

Anyone in AF with RVR (Rapid Ventricular Rate) who is unstable needs electrical cardioversion. These are the four signs/symptoms of instability: 

  1. Altered mental status
  2. Ischemic chest discomfort
  3. Acute heart failure
  4. Hypotension
In addition, these two sub-groups are also considered for electrical cardioversion:
  1. AF with rates b/w 250-300 and bizarre QRS morphology (suggesting WPW syndrome)
  2. When medications fail in stable patients


Caveat:  Patients who look well with a BP around 80-90 systolic may be treated with medications to control the rate/rhythm. If they look unwell with the same numbers, then do Synchronised Cardioversion. Don't stick to that arbitrary cut off of 90/60 for everyone. Decision to electrically cardiovert is based on symptoms and clinical appearance. 

Electrical cardioversion is the quickest way to rate control in AF because it converts the patient back to sinus rhythm. Patients with chronic AF will eventually go back to an irregular rhthym. Thus ED management is primarily based on rate control unless they are unstable. 

Procedural sedation and carries a risk of embolic events and cardiac arrhythmias. Analgosedation (Not just sedation) is recommended during electrical cardioversion. Give them some sedation with propofol/etomidate/BZD and add fentanyl/morphine for pain relief. Propofol/etomidate/BZD do not provide any pain relief. 



When doing Synchronised DC Cardioversion, 
  • Start with higher energy gives a better success rate
  • Consider anterior-posterior pad placement for biphasic defibrillators
  • Time with patient’s respiratory cycle, shock during full expiration  

Rate Control v/s Rhythm Control
Multiple studies have shown no difference in all cause/cardiovascular mortality or stroke rate among patients treated with rate or rhythm control. 50% of new AF spontaneously convert to Sinus Rhythm within 48 hours. Pro- longed outpatient attempts to establish or maintain a sinus rhythm in patients with recurrent atrial fibrillation do not offer a clear benefit compared with rate control. AF can present in these 6 ways:
  

1. AF with WPW (Rates more than 200 with bizarre QRS complexes)
Synchronised electrical cardioversion is the primary treatment for unstable patients with an accessory pathway or those who present with a very rapid heart rate, even if stable. Stable patients can be treated with Sync. Cardioversion/Procainamide. Unstable patients certainly need immediate Sync. Cardioversion. 





2. Acute (New-onset) Hemodynamically Stable AF - It is reasonable to start with rate control to relieve symptoms. A good history is needed to figure out the cause (Sepsis, PE, Thyrotoxicosis) and start specific treatment. Almost 50% convert to Sinus Rhythm spontaneously within 48 hours. 

Pharmacological Cardioversion with (Amiodarone/Procainamide/Ibutilide) is also an acceptable option. Before pharmacological cardioversion, ensure that QTc and serum electrolytes are within normal ranges as rhythm control medication prolong QTc and increase the risk of Torsades. 

Patients may not be able to correctly identify the time of onset of AF based on their symptoms and the use of TEE has shown that a clot may be present in the atrium up to 13% of the time in patients with AF < 72 hours duration. Therefore, it is recommended to give unfractioned heparin concurrently (unless contraindicated) by an initial IV bolus injection followed by a continuous infusion. Thereafter, oral anticoagulation (INR 2.0-3.0) should be provided for at least 4 weeks.

Bottomline - Any unstable patient needs immediate electrical cardioversion regardless of acute or chronic AF. If acute, give heparin and do synchronised electrical cardioversion. Very often Chronic AFs are already on oral anti-coagulation obviating the need for concurrent heparin. 

3. Acute Hemodynamically Unstable AF - Treat with Synchronised electrical cardioversion. Always make your best attempts to provide some analgesia and sedation prior to delivering shock. 

There is a another school of thought that assumes that hypotension (unstable) in Rapid AF is due to the rapid ventricular rate. Thus giving rate/rhythm control medications will slow down the heart allowing adequate ventricular filling which will improve the CO/blood pressure. Therefore, it sounds reasonable to try medications but be prepared for cardioversion if medications fail. 

Other causes of hypotension should be investigated before concluding that the rate is causing the hemodynamic deterioration.

4. Chronic Hemodynamically Stable AF -R his is the most common subgroup that presents to the ED with fast ventricular rates. Rate control with CCB/BB/Digoxin/Mg. Amiodarone is falling out of favour due to significant side effects. Check out what Amal Mattu thinks about Amiodarone. 




5. Chronic Hemodynamically Unstable AF - Treat with electrical cardioversion. Check if they are on oral anti-coagulation. If not on oral anticoagulants, give concurrent heparin. The risk of thromboembolism is high as this is long standing AF and thus this subgroup is often treated with rate-control medications to avoid Sync. Cardioversion and subsequent risk of thrombo-embolism. Again, those who support rate-control with drugs use for unstable patients argue that rate control with medication will revert the signs of instability. 


6. Unstable AF who fails Electrical Cardioversion
This is a grey area. One way to reduce hypotension includes pretreatment with push-dose phenylephrine (50-200 mcg every 1-2 minutes) to a goal diastolic blood pressure > 60 mm Hg. IV Calcium (5-10 mL of calcium gluconate) may reduce  hypotensive effects of verapamil without compromising the rate controlling property. Following pretreatment with Phenylephrine and Calcium, slow them down with verapamil (2.5 mg/min continuous drip until heart rate < 100 beats/min (or 50-mg total dose) or amiodarone (150-mg bolus).

Phenylephrine/Calcium premedication prior to Verapamil can be considered for any unstable patient. 


Another way is to treat with antiarrhythmic agent such as amiodarone, ecainide, ibutilide, propafenone, or stall and re-attempt  electrical cardioversion. 

Choosing a Rate-Controlling Agent: With rate-controlling medications We try to prolong the atrioventricular refractory periods, thus slowing atrioventricular nodal conduction.


  • BB: Often the first line medication to treat AF in the absence of pre-excitation syndromes. Beta blockers should be the first drug of choice in patients with congestive heart failure or left ventricular dysfunction, post-operative AF, hypertension, thyrotoxicosis, and acute coronary syndromes. Use BB with caution in patients with hypotension or acutely decompensated heart failure.
  • CCB: CCBs are another first-line medications for the treatment of acute AF. CCB are preferred over BB on COPDs. Diltiazem tends to be more popular than verapamil for acute rate control, as verapamil has more potent negative inotropic and vasodilator effects that may lead to hypotension. 
  • Digoxin: Digoxin has both negative chronotropic and positive inotropic effects, which is particularly useful in patients with congestive heart failure, but the onset of action may take few hours. It is especially useful in hypotensive patients. Digoxin has a synergistic effect with BB/CCB. Verapamil may increase the concentration of digoxin.
  • Mg: Magnesium decreases conduction through the AV node but Mg use is most often recommended only as an adjunctive therapy. Magnesium may also promote conversion to sinus rhythm, with some studies showing 50% to 60% of patients converted to sinus rhythm.



Choosing a Rhythm Control Agent

Options include: Procainamide, Amiodarone, Flecainide, Ibutilide. 


Flecainide and propafenone are reserved for patients without significant structural heart disease, hypertension, ischemia, or heart failure. 

For Preexcitation syndromes such as Wolff-Parkinson White syndrome, the use of AV nodal blocking agents such as beta blockers, calcium channel blockers, and digoxin may induce ventricular brillation and are contraindicated.

Procainamide slows conduction through the accessory pathway and prolong the refractory period in the bypass tract, and they can be safely used in patients in rapid AF with Wolff-Parkinson-White syndrome. Procainamide is safer than Amiodarone in WPW Syndrome. 


Summary:
Management of AF is quite variable and largely dependent on local protocols and physician preferences. From ED management standpoint, rate control remains our priority and sync electrical Cardioversion is reserved for unstable patients, stable patients who do not show improvement with medications alone and for stable patients with an ECG suggestive of an accessory pathway. 

Whenever you try medications for unstable patients, be prepared for electrical cardioversion as these medications have the potential to worsen hypotension. 


  1. AF with WPW - Sync Cardioversion for stable/unstable, Procainamide for stable
  2. Acute Stable AF - Rate Control with BB/CCB/Dig/Mg and wait for spontaneous cardioversion or Rhythm control with Procainamide/Amio
  3. Acute Unstable AF - Sync Cardioversion with concurrent heparin, May try rate control first
  4. Chronic Stable AF - Rate control with BB/CCB/Digoxin/ Mg
  5. Chronic Unstable AF - Sync. Electrical Cardioversion with heparin (if not on oral anti-coags), or rate control with BB/CCB/Mg/Digoxin, Consider phenylephrine/Calcium to premedicate and administer verapamil/amiodarone drip.  
  6. AF Refractory to Cardioversion - After failed shocks, try medications and then shock again or Use phenylephrine/Calcium to premedicate and administer verapamil/amiodarone drip. 

Posted by:


              
     Lakshay Chanana
     
     Speciality Doctor
     Northwick Park Hospital
     Department of Emergency Medicine
     England

     @EMDidactic




                    

Hypothermic patient in ED





Hypothermia is defined as a temperature of <35C. It is a common presentation in the Emergency Departments esp in elderly population with ? Sepsis. Geriatric population is prone to suffer from hypothermia due to poor mobility and altered temperature perception in addition to the environmental factors. Let's look at the common causes of hypothermia:
Causes

  • Environmental (often Accidental)
  • Hypoglycaemia (hypothalamic dysfunction secondary to glucopenia)
  • Hypothyroidism
  • Hypopituitarism
  • Hypoadrenalism
  • Hypothalamic Dysfunction (Tumor, Stroke, Infarction)
  • Sedatives and Alcohol
  • Sepsis
  • Massive Blood Transfusion
  • Burns and Exfoliative Dermatitis




Systemic Effects

CVS - BP and CO rise initially but later there is a phase of CVS depression and a general slow down of metabolism. This may lead to hypotension which is exacerbated by concomitant hypovolumia. Hypothermia usually causes bradyarrythmiats such as slow AF, sinus bradycardia, J waves, AV blocks, QTc prolongation on EKG. The management should focus on rewarming rather than administering anti-arrythmics. Also, hypothermic myocardium is irritable, and ventricular fibrillation may be induced by rough handling of the patient.

RS - Decrease O2 utility and less CO2 production. Patients may show a respiratory alkalosis or acidosis due to CNS depression. Lactate may be elevated due to shivering and hypoxia. There is also depression of gag and cough reflex making aspiration likely. Hypothermia causes a leftward shift of the oxyhemoglobin dissociation curve and thus impairs oxygen release to tissues. 

CNS - Confusion, lethargy, coma and unreactive pupils. There is decreased blood flow and cerebral protection against ischemic damages. Do not pronounce them dead until you are 100% sure. Use ECHO, ECG and Clinical judgment before you declare them dead.

Renal - Cold induced diuresis which contributes to volume loss, risk of rhabdo and AKI. 

Haematological - Hemoconcentration, thrombotic and embolic complications, DIC and Hypothermia induced coagulopathy. This coagulopathy may not be evident of blood tests but seen clinically. 


Investigations
  • Blood Glucose
  • Septic Screen (including CXR, Urine)
  • TSH
  • Creat Kinase
  • ECG
  • Heat CT (Consider after a period of observation - Every elderly with hypothermia does not need a Head CT)

Management
  • ABCs
  • Take up to 30 seconds to assess before commencing chest compressions - Use ECHO, feel for pulses and watch for respiratory movements. Handle them gently to avoid irritating the myocardium. If it is a hypothermic arrest then administer epinephrine every 6-10 minutes unless they are re-warmed and hypothermic arrhythmias may not respond to Cardioversion. Focus on warming in such a scenario
  • Warm O2 and Warm fluids
  • External Warming Blankets. Rapid rewarming is rarely needed. There are other rescue intensive and invasive methods such as pleura/peritoneal/GI/Bladder lasagne and ECMO. 
  • Arrhythmias - Rewarm then and only then think about anti-arrythmics
  • Antibiotics if concerned about Sepsis
  • Parenteral Thiamine for critically ill/malnourished/alcoholics/unexplained lactic acidosis
  • Steroids for septic shock refractory to one vasopressor/adrenal crisis and severe hypothyroidism

Unless there is obvious evidence, death in hypothermia must be defined as a failure to revive with rewarming (at least a core T of 30C)

Take Home:
Think beyond sepsis and environmental causes of hypothermia, think Endocrine causes!

Posted by:

              
     Lakshay Chanana
     
     Speciality Doctor
     Northwick Park Hospital
     Department of Emergency Medicine
     England

     @EMDidactic



The Intractable Migraneous Headache

Migraine headaches results from dysfunction of brainstem pathways that normally modulate sensory input, with disordered activity of blood vessels. This leads to neurogenic inflammation in pain-sensitive arteries, the dura, and meningeal tissues, and promotes local vasodilatation. Medications such as sumatriptan and ergot derivatives cause vasoconstriction and relieve the symptoms. These triggers stimulate trigeminovascular axons causing pain and the release of vasoactive neuropeptides from perivascular axons. 


Clinical Presentation
  • Headache that lasts from 4 to 72 hours
  • Aggravation by routine physical activity
  • Classically unilateral and pulsating (May not be unilateral)
  • a/w Nausea, vomiting, and photophobia or photophobia 
  • May have Scalp Tenderness 
  • Aura (most common are visual auras with flashes of lights)

Key Q - Is your headache similar to your usual migraine headaches? If the news is no, then a different cause should be suspected. 




Treatment Options for Migraine
  • Acetaminophen - Patients with diagnosed migraine often try paracetamol before arriving to the EDs. There is no harm in adding Paracetamol to routine migraine therapy.
  • FluidsDehydration is a known trigger of migraine. Persistent nausea and vomiting further exacerbates the migraine. Adequate hydration might improve patient malaise and help those who are dehydrated.
  • Anti-emetics - Parenteral metoclopramide, chlorpromazine, and prochlorperazine (Stemetil) all have demonstrated efficacy in randomized trials as monotherapy for acute migraine. Antiemetic medications are efficacious and are recommended for acute migraine in the ED. To reduce the risk of akathisia, diphenhydramine should be included. (Diphenhydramine does not prevent Metoclopramide induced dystonia)
  • Oxygen - "High-flow" oxygen has been studied in migraine headaches. When compared with placebo, oxygen used for 15 min was more effective in pain relief with no significant adverse events.
  • Steroids - Steroids prevent the lingering of attacks and recurrence as well. Everyone with a migraine attack should receive dexamethasone 10mg IV/IM or a 3 day course of presdqisolone unless there is an obvious contraindication. 
  • NSAIDs - NSAIDs are effective in treating acute migraine. Ketorolac is a potent pain killer which often works for migraine.

  • Triptans - Evidence suggests that SC delivery is fastest and most effective route. Common side effects include injection site reactions, dizziness, and paresthesias. Triptans are contraindicated in cardiovascular disease, pregnancy, basilar migraines, Prinzmetal angina, and ischemic stroke, and with the use of ergotamines within the previous 24 hours. Studies have also suggested that triptan therapy is less effective in patients with prolonged and severe migraine. Triptans are best reserved for patients who present within 1-2 hours of headache. Given the side effect profile, lack of efficacy in severe migraine, and relative contraindications, triptan use in the ED is of limited value. 
  • Butyrophenones - (haloperidol and droperidol). RCTs have demonstrated efficacy of haloperidol and droperidol mono therapy. However, these drugs have been associated with frequent side effects (somnolence, akathisia, anxiety) and also prolong QTc interval. These are generally reserved for rescue therapy in refractory migraine. 
  • Ergot Alkaloids - Dihydroergotamine (DHE), a 5-HT1B/1D serotonin receptor agonist which highly effective in relieving headaches. However, DHE causes vomiting in a significant proportion of patients. Patients therefore should be pretreated with an antiemetic such as metoclopramide or prochlorperazine.
  • Opioids - Use opioids only as the last sort for refractory headache. When compared with NSAIDs, DHE, and antiemetic medications, opioids are less effective for migraine. The frequent use of opioids in chronic and recurrent headache conditions may lead to adverse effects and may even exacerbate headaches.
  • Propofol - Evidence for using propofol is not robust but it is again something to consider when everything else fails. Follow the procedural sedation protocol and doe as 10-20 mg IVP every 3-4 minutes up to 1 mg/kg. Our aim is mild sedation, not apnea.
  • Magnesium - Magnesium is ideally used for refractory migraine, migraine patients with true aura, those with hypoMg. Administer 2 g IV Mg over 20min. Evidence for the use of Migraine is still conflicting though. 

Bottomline: It is reasonable to start with fluids/O2, Metoclopramide. Do not forget to add steroids. Add Acetaminophen/NSAIDs if symptoms persist. Other  potential options (Ergot Alkaloids/Mg/Propofol, Ganglion Blocks) are all based on your comfort and local protocols. Opioids are your last option. 


References:
  • Singhal AB, Maas MB, Goldstein JN, et al. High-flow oxygen therapy for treatment of acute migraine: A randomized crossover trial. Cephalalgia. 2016 May 20.
  • Balbin JE, Nerenberg R, Baratloo A, Friedman BW. Intravenous fluids for migraine: a post hoc analysis of clinical trial data. Am J Emerg Med. 2016 Apr;34(4):713-6.
  • Bigal ME, Bordini CA, Tepper SJ, Speciali JG. Intravenous magnesium sulphate in the acute treatment of migraine without aura and migraine with aura. A randomized, double-blind, placebo-controlled study. Cephalalgia. 2002 Jun;22(5):345-53.
  • Colman I, Friedman BW, Brown MD, Innes GD, Grafstein E, Roberts TE, Rowe BH. Parenteral dexamethasone for acute severe migraine headache: meta-analysis of randomised controlled trials for preventing recurrence. BMJ. 2008 Jun 14;336(7657):1359-61.
  • Colman I, Rothney A, Wright SC, Zilkalns B, Rowe BH. Use of narcotic analgesics in the emergency department treatment of migraine headache. Neurology. 2004 May 25;62(10):1695-700.
  • Friedman BW, Bender B, Davitt M, Solorzano C, Paternoster J, Esses D, Bijur P, Gallagher EJ. A randomized trial of diphenhydramine as prophylaxis against metoclopramide-induced akathisia in nauseated emergency department patients. Ann Emerg Med. 2009 Mar;53(3):379-85.
  • Friedman BW, Greenwald P, Bania TC, Esses D, Hochberg M, Solorzano C, Corbo J, Chu J, Chew E, Cheung P, Fearon S, Paternoster J, Baccellieri A, Clark S, Bijur PE, Lipton RB, Gallagher EJ. Randomized trial of IV dexamethasone for acute migraine in the emergency department. Neurology. 2007 Nov
  • Regan LA, Hoffman RS, Nelson LS. Slower infusion of metoclopramide decreases the rate of akathisia. Am J Emerg Med. 2009 May;27(4):475-80.
  • Soleimanpour H, Taheraghdam A, Ghafouri RR, Taghizadieh A, Marjany K, Soleimanpour M. Improvement of refractory migraine headache by propofol: case series. Int J Emerg Med. 2012 May 15;5(1):19.
  • Taggart E, Doran S, Kokotillo A, Campbell S, Villa-Roel C, Rowe BH. Ketorolac in the treatment of acute migraine: a systematic review. Headache. 2013 Feb;53(2):277-87.